Non-Alcoholic Fatty Liver Disease in Overweight Children: Role of Fructose Intake and Dietary Pattern

Abstract

The role of nutrition and diet in the development of non-alcoholic fatty liver disease (NAFLD) is still not fully understood. In the present study, we determined if dietary pattern and markers of intestinal permeability differ between overweight children with and without NAFLD. In addition, in a feasibility study, we assessed the effect of a moderate dietary intervention only focusing on nutrients identified to differ between groups on markers of intestinal barrier function and health status. Anthropometric data, dietary intake, metabolic parameters, and markers of inflammation, as well as of intestinal permeability, were assessed in overweight children (n = 89, aged 5–9) and normal-weight healthy controls (n = 36, aged 5–9). Sixteen children suffered from early signs of NAFLD, e.g., steatosis grade 1 as determined by ultrasound. Twelve children showing early signs of NAFLD were enrolled in the intervention study (n = 6 intervention, n = 6 control). Body mass index (BMI), BMI standard deviation score (BMI-SDS), and waist circumference were significantly higher in NAFLD children than in overweight children without NAFLD. Levels of bacterial endotoxin, lipopolysaccharide-binding protein (LBP), and proinflammatory markers like interleukin 6 (IL-6) and tumor necrosis factor α (TNFα) were also significantly higher in overweight children with NAFLD compared to those without. Total energy and carbohydrate intake were higher in NAFLD children than in those without. The higher carbohydrate intake mainly resulted from a higher total fructose and glucose intake derived from a significantly higher consumption of sugar-sweetened beverages. When counseling children with NAFLD regarding fructose intake (four times, 30–60 min within 1 year; one one-on-one counseling and three group counselings), neither alanine aminotransferase (ALT) nor aspartate aminotransferase (AST) activity in serum changed; however, diastolic blood pressure (p < 0.05) and bacterial endotoxin levels (p = 0.06) decreased markedly in the intervention group after one year. Similar changes were not found in uncounseled children. Our results suggest that a sugar-rich diet might contribute to the development of early stages of NAFLD in overweight children, and that moderate dietary counseling might improve the metabolic status of overweight children with NAFLD.

Adipokines and Endotoxemia Correlate with Hepatic Steatosis in Non-Alcoholic Fatty Liver Disease (NAFLD)

“…We have previously shown that NAFLD predisposes to increased levels of endotoxin in children and adults with NAFLD [20,26,27] and these findings are again reflected in the current study. Importantly, we are able to recapitulate observations related to endotoxemia and link these to the dietary composition in a prospectively enrolling nutritional trial [27]. In contrast to endotoxin, no differences in LBP were observed in patients and healthy volunteers.…”

Analysis of the dietary factors associated with suspected pediatric nonalcoholic fatty liver disease and potential liver fibrosis: Korean National Health and Nutrition Examination Survey 2014-2017

“…This finding is supported by previous studies showing that the ingestion of a diet excessively rich in carbohydrates, particularly fructose, causes de novo lipogenesis, which may induce hepatic fat accumulation [10,49]. The consumption of sugar-sweetened beverages is associated with metabolic syndrome and fatty liver in adult and pediatric patients [50,51]. In contrast, protein intake exerts a positive effect on NAFLD by reducing fat deposition and plasma cholesterol levels [17,20].…”

Consumption of Sugar-Sweetened Beverages in Paediatric Age: A Position Paper of the European Academy of Paediatrics and the European Childhood Obesity Group

“…Many health problems have been linked to the high consumption of sweetened beverages, such as caries and enamel erosion, short sleep duration, hyperactivity, increased blood pressure and non-alcoholic fatty liver disease (NAFLD) [22,23].…”